Although different protozoan and helminthic parasites have been shown to activate different mechanisms of innate immunity, these organisms are often able to survive and replicate in their hosts because they are well adapted to resisting host defenses. The principal innate immune response to protozoa is phagocytosis, but many of these parasites are resistant to phagocytic killing and may even replicate within macrophages. Some protozoa express surface molecules that are recognized by TLRs and activate phagocytes. Plasmodium species (the protozoa that are responsible for malaria), Toxoplasma gondii (the agent that causes toxoplasmosis), and Cryptosporidium species (the major parasite that causes diarrhea in HIV-infected patients) all express glycosyl phosphati-dylinositol lipids that can activate TLR2 and TLR4. Phagocytes may also attack helminthic parasites and secrete microbicidal substances to kill organisms that are too large to be phagocytosed. However, many helminths have thick teguments that make them resistant to the cytocidal mechanisms of neutrophils and macrophages, and they are too large to be ingested by phagocytes. Some helminths may activate the alternative pathway of complement, although as we shall discuss later, parasites recovered from infected hosts appear to have developed resistance to complement-mediated lysis.
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